Chronic inflammation (CEO/CP) disrupts the bridge: In CEO, testicular inflammation may initially elevate testosterone (compensatory Leydig cell response) [11,18] and later cause hypogonadism (29.2% of CEO patients had testosterone <300 ng/dL). In CP, systemic cytokines (IL-1β, TNF-α) suppress the hypothalamic-pituitary-gonadal (HPG) axis, lowering testosterone and exacerbating both semen abnormalities [14,13] and sexual dysfunction [14,18]. This evidence concerns the gene IL1B and hypogonadism.